PHAR1014 W1 AKD Summary

Explain & compare the pathophysiology, symptoms presentation of acute kidney disease
Acute Kidney Injury (AKI): A decrease in glomerular filtration over hours to weeks
Assessed by looking at:
 Serum Creatinine
 Urea
 Urine output
Three classifications, based on how it happened:
1) Prerenal
2) Intrinsic/Intrarenal
3) Postrenal

AKI-Broad Classification
Pre-renal (~40-80%) Reduced Renal Perfusion
Something has decrease fluid or blood flow to
kidney
Intra-renal (within kidney) (~40%) Intrinsic damage to the kidney cells and
structure supporting kidney cells

Post-renal (5-10%) (Leaving the kidney) Obstruction of Urine Outflow

E.g. Prostate, cancer, stones

Patient Presentation
 Uncommon for an outpatient to present with AKI alone
 AKI is diagnosed before a patient notices symptom
 Often AKI occurs in patients who are ALREADY very unwell

Signs and symptoms might include:

 Change in urinary habits (Lots, little, None)
 Weight gain/fluid retention
 Coloured foamy urine (indicate proteins in urine)

Detail the course of acute kidney injury, explaining the likely consequences
There are 2 classification of AKI
 Site of cause (Pre-renal, Intrinsic, Post Renal)
 Amount of Urine being produced:
 Oliguric (LESS urine production)
 Anuria (NO urine)
 Non-oliguric
 Polyuric (EXCESSIVE urine production)
The most typical course of AKI
(AKIOliguriaPolyuriaRecovery)

1) Something causes AKI (hence kidney stop working)

2) Kidneys attempt to increase perfusion (blood flow) by vasoconstriction, which leads to
Oliguria (minimise fluid loss)
3) Kidney gradually recover (ability to concentrate urine  leads to Polyuria)

Identify risk factors and causes of acute kidney injury

AKI risk factors

 Advanced age
 Infection
 Respiratory or Cardiovascular disease
 Recent surgery
 Pre-existing chronic kidney disease

Pre-renal AKI
Renal failure caused by a LACK of perfusion due to LACK of pressure through the kidney

Causes:
 Fluid Loss (Dehydration. Diuretics, bleeding)
 Hypotension
 Constriction of Afferent Arteriole
 Dilation of Efferent Arteriole
 Drugs

In a normal Kidney DRUG Causes of Prerenal AKI

 NSAID  Cause vasoconstriction at Afferent arterioles
(inhibit the action of Prostaglandin)  Decreasing pressure across Glomerulus

Loop Diuretics  Cause decreased in fluid volume

( decreasing Fluid as it gets rid of fluid)  Decreasing pressure across Glomerulus

ACE-Inhibitor  Cause vasodilation at efferent arteriole

(inhibit the action of RAAS thus inhibit  Decreasing pressure across Glomerulus
constriction)

In combination: Double or “triple-whammy

 taking 2 or more of the identified drugs was associated with significant renal impairment

Intrinsic (intra-renal) AKI

Caused by damage to the
Glomerulus or kidney itself
Causes:
 Vascular damage (e.g. vasculitis)
 Glomerular damage
 Acute Tubular Necrosis (dead tubular Cell)
 Acute interstitial nephritis
 Inflammation of the supporting structure nephron
 (e.g. Penicillin)

Post-renal AKI
Caused by obstruction of Causes:
Urine Flow  Bladder outlet obstruction
 e.g. large prostate
 Anti-cholinergic medicines (urinary retention)
 Tubule Obstruction
 e.g. kidney stones

Aciclovir: can cause crystallisation hence tell patient to drink lots of

water
Kidney stone
Result of Ca2+ salt crystallising
Can cause extreme pain  managed with analgesics (esp. NSAID or Opioids)

Preventing Kidney stone in the Long term

1) Thiazide Diuretics: reduce Ca2+ Excretion
2) Low Salt diet: High Serum Na+ promotes Ca2+ excretion

Discuss the management of acute kidney disease

 Aim to avoid it becoming chronic kidney disease
 Patient with AKI (minimise further renal injury)

Avoid Nephrotoxic agents Examples

Drugs can induce kidney disease
Manage Fluid appropriately
Body will not be able to produce urine, so
patients can become overloaded
 Drugs that decrease perfusion to the
kidney (Diuretic, ACE-I, NSAID)
 Drugs directly toxic to the kidney
Critical to ensure
 Adequate fluid to maintain kidney
perfusion
 Not an excess of fluid

NOTE: Loop diuretics are not appropriate

Review all Medication and doses
Important for drugs which are renally cleared
 Renal replacement therapy may be
required
In AKI various changes can happen
 Changes in Clearance
 Changes in Volume of distribution

Recovery from AKI

 Renal function declines with age
 Episodes of AKI speed up the decline in renal function
 100% recovery (if AKI managed early)
 Long term problems more likely if there has been acute tubular necrosis (cell death)
 Tubule cells have died then regeneration of new cells need to occur
 Recovery may not be 100% complete- Can lead to chronic kidney disease